Environmental Science-Processes & Impacts
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2025
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IF 3.9
Xiaomin Ren,Jianying Wang,Fenqing Zhao,Pingping Zhang,Huan He,Zhixiang Xu,Bin Huang,Xuejun Pan
Previous studies have indicated that 6:2 chlorinated polyfluoroalkyl ether sulfonate (6:2 Cl-PFAES), a substitute for perfluorooctane sulfonate (PFOS), caused disruptions in glucose metabolism, but its toxicological mechanisms remain unclear. Pancreatic β cells are responsible for regulating glucose metabolism. This study used mouse insulinoma β cells (β-TC-6) to study the toxic effects of 6:2 Cl-PFAES and elucidate its potential mechanisms. Through cell counting kit-8, trypan blue staining, and apoptosis assays, we found that 6:2 Cl-PFAES showed toxicity to β-TC-6 cells, even surpassing that of PFOS. Mechanistic studies demonstrated that 6:2 Cl-PFAES induced oxidative stress by ascendant levels of reactive oxygen species (ROS) and malondialdehyde (MDA), alongside increased superoxide dismutase (SOD) activity. The oxidative stress-inducing capability of 6:2 Cl-PFAES was stronger than PFOS. Co-exposure with N-acetyl-L-cysteine (NAC), as the ROS scavenger, which obviously reduced the degree of cell apoptosis and the production of ROS, highlighting oxidative stress as a crucial mechanism of 6:2 Cl-PFAES-induced cell death. Transcriptomic analysis further revealed that 6:2 Cl-PFAES affected genes association with the oxidative phosphorylation pathway, confirming the oxidative stress effect, and altered diabetes-related genes expression, suggesting a heightened risk of diabetes. This study provides insights into the toxicity of 6:2 Cl-PFAES on β cells and its potential risks on glucose metabolism disruption.
研究领域:
毒理学
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分子生物学
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环境健康科学
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高影响因子
Scientific Reports
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2025
·Vol. 15
·期 1
·1-16
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IF 3.9
Wu Yongming,Pei Kexuan,Zhou Jiayu,Xiong Jianzhong,Liu Yu,Li Panrong,Li Fangfei,Wang Jiaqi,Liu Xiangmin,Deng Mi,Wu Chenxi
A novel substitute for perfluorooctane sulfonate (PFOS), 6:2 Chlorinated polyfluoroalkyl ether acid (6:2 Cl-PFAES, F-53B), has been widely used in the electroplating and firefighting industries, raising concerns due to increasing environmental prevalence. This study systematically investigated the adsorption characteristics of F-53B by coconut shell activated carbon (CSAC) and elucidated the underlying mechanisms through adsorption kinetics, isotherm modeling, and multi-scale characterization. Results show that the maximum adsorption capacity of CSAC for F-53B reached 261.64 mg/g, with the process best described by the pseudo-second-order kinetic model (R 2 > 0.97) and the Langmuir isotherm (R 2 > 0.94). Intraparticle diffusion modeling revealed a three-stage adsorption sequence: surface adsorption (0–2 h), pore diffusion (2–8 h), and dynamic equilibrium (8–48 h). Solution pH influenced adsorption efficiency by regulating surface charge. Under acidic conditions (pH < point of zero charge, pHzpc = 4.49), strong electrostatic interactions between protonated CSAC surfaces and anionic F-53B resulted in an 85% removal efficiency. In contrast, alkaline conditions (pH > 7) led to a 70% reduction in adsorption efficiency ( p < 0.05) due to electric repulsion. The microporous-dominated structure of CSAC (specific surface area: 857.69 m 2 /g; pore volume: 0.34 cm 3 /g) facilitated synergistic adsorption mechanisms. Oxygen-containing functional groups (C-O, -OH) promoted hydrogen bonding and hydrophobic interactions, enhancing F-53B adsorption. Besides, CSAC is optimized for emergency scenarios, it achieves 99.9% removal efficiency for 1 mg/L F-53B within 8 h at room temperature, with a maximum capacity of 261.64 mg/g; also, it maintains > 85% removal efficiency under wide pH conditions and tolerates coexisting ions (e.g., Cl − , SO 4 2− , Ca 2+ ).This study highlights the multi-mechanistic synergy of CSAC in theremoval of F-53B, providing theoretical foundations and technical insights for biochar-based remediation of emerging contaminants.
研究领域:
环境科学
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化学工程
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水处理
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吸附技术
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材料科学
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ENVIRONMENTAL SCIENCE & TECHNOLOGY
·
2026
·
IF 11.3
Jinchen Jiang,Haixia Meng,Zhenhao Shu,Nannan Zhao,Xiaojun Lin,Jianglan Li,Minjun Qin,Siyu Wu,Lianglin Qiu
As an emerging alternative to perfluorooctanesulfonate (PFOS), 6:2 chlorinated polyfluoroalkyl ether sulfonate (6:2 Cl-PFAES) is associated with male reproductive disorders, yet its testicular targets and mechanisms remain unclear. This study combined in vivo exposure of male C57BL/6J mice (0, 4, 40, and 400 μg/L for 18 weeks) and in vitro assays in primary Leydig cells to demonstrate that 6:2 Cl-PFAES dose-dependently reduced sperm count and serum/testicular testosterone, accompanied by testicular interstitial vacuolation. Transcriptomics and metabolomics demonstrated the concurrent significant enrichment of autophagy pathways and disruption of lipid metabolism. Mechanistically, 6:2 Cl-PFAES suppressed expressions of Sirtuin 1 (SIRT1), ras-related GTP binding protein 7 (RAB7), and deacetylation of forkhead box class O1 (FOXO1), thereby impairing lipophagy flux and promoting lipid droplets accumulation. Molecular docking indicated comparable binding affinity of 6:2 Cl-PFAES and PFOS to SIRT1 (−10.4 kcal/mol), and further research demonstrated that 6:2 Cl-PFAES reduced the deacetylation activity of SIRT1. Crucially, Sirt1 overexpression in transgenic mice (Sirt1TG) or pharmacological activation of SIRT1 (SRT1720) and RAB7 (ML-098) rescued testosterone synthesis and restored lipophagy flux. This study identifies the SIRT1–FOXO1–RAB7 axis as a core target for 6:2 Cl-PFAES-induced suppression of testosterone biosynthesis via lipophagy dysregulation, providing critical molecular insights for assessing the reproductive risks of PFOS alternatives.
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